PKU, Learning, and models of mental retardation

Strupp, Barbara J.; Levitsky, David A.; Blumstein, Lisa

doi:10.1002/dev.420170202

Cited by 26 publications

(7 citation statements)

References 43 publications

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“…The HP and control groups did not differ in the rate at which they mastered the first discrimination problem (see Figure 1). This lack of impairment in the rate of learning a simple association is consistent with the existing literature concerning both experimental PKU in animals (see Strupp, Levitsky, & Blumstein, 1984) and mental retardation in humans (see Brooks et al, 1987). The control group did, however, require significantly fewer trials to reach criterion in the second (F(1,71) = 4.39; p = .019, one-tailed) and third (F(1,71) = 4.45, p = .019, onetailed) discrimination problems than did the HP group, a difference in learning rate that was also apparent in an analysis of all three problems combined (F( 1,160) = 5.68, p = .009, one-tailed).…”

Section: Learning-to-learnsupporting

confidence: 91%

Cognitive profile of rats exposed to lactational hyperphenylalaninemia: Correspondence with human mental retardation

Strupp

Himmelstein

Bunsey

et al. 1990

Developmental Psychobiology

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The present study was designed to provide further information on the enduring cognitive effects of experimental phenylketonuria (PKU) in rats, produced by the administration of alpha-methylphenylalanine and phenylalanine on postnatal days 3-21. These rats evidenced: (1) impaired learning set formation, (2) stimulus perseveration, particularly after an error, and (3) difficulty in utilizing the less salient features of their environment in mastering discrimination problems. In contrast, long-term memory function and the ability to form simple associations did not differ from controls. This pattern of intact and impaired cognitive functions bears remarkable similarity to that of mentally retarded humans and neonatally hyperphenylalaninemic rhesus monkeys, thus affirming the use of rats to study mental retardation. In addition, possible reasons for the mildness of the impairments commonly observed in animal models of severe mental retardation syndromes are discussed. We suggest that transfer of learning paradigms that assess the animal's ability to use information acquired in other problems are more likely to uncover significant cognitive impairments in such models than are procedures that test only the animals' ability to solve a single problem.

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Section: Learning-to-learnsupporting

confidence: 91%

Cognitive profile of rats exposed to lactational hyperphenylalaninemia: Correspondence with human mental retardation

Strupp

Himmelstein

Bunsey

et al. 1990

Developmental Psychobiology

Self Cite

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“…Rats will exhibit a greater preference for a novel substance when they are allowed to observe another rat that has been exposed to the substance [66–68]. This demonstrator-observer paradigm has been extended to assess effects related to alcohol preference, but interestingly, alcohol odor preference was only increased in adolescent rats that had been able to interact with an alcohol-intoxicated peer, not in those that were exposed to an anesthetized rat that had also received alcohol [69].…”

Section: Social Facilitation Of Alcohol Intakementioning

confidence: 99%

Biological Contribution to Social Influences on Alcohol Drinking: Evidence from Animal Models

Anacker¹,

Ryabinin²

2010

IJERPH

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Social factors have a tremendous influence on instances of heavy drinking and in turn impact public health. However, it is extremely difficult to assess whether this influence is only a cultural phenomenon or has biological underpinnings. Research in non-human primates demonstrates that the way individuals are brought up during early development affects their future predisposition for heavy drinking, and research in rats demonstrates that social isolation, crowding or low social ranking can lead to increased alcohol intake, while social defeat can decrease drinking. Neurotransmitter mechanisms contributing to these effects (i.e., serotonin, GABA, dopamine) have begun to be elucidated. However, these studies do not exclude the possibility that social effects on drinking occur through generalized stress responses to negative social environments. Alcohol intake can also be elevated in positive social situations, for example, in rats following an interaction with an intoxicated peer. Recent studies have also begun to adapt a new rodent species, the prairie vole, to study the role of social environment in alcohol drinking. Prairie voles demonstrate a high degree of social affiliation between individuals, and many of the neurochemical mechanisms involved in regulation of these social behaviors (for example, dopamine, central vasopressin and the corticotropin releasing factor system) are also known to be involved in regulation of alcohol intake. Naltrexone, an opioid receptor antagonist approved as a pharmacotherapy for alcoholic patients, has recently been shown to decrease both partner preference and alcohol preference in voles. These findings strongly suggest that mechanisms by which social factors influence drinking have biological roots, and can be studied using rapidly developing new animal models.

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“…Both PKU as well as its associated animal models are characterized by the development of severe cognitive impairments such as a learning deficit. 36,37 The mechanism(s) whereby hyperphenylalaninemia produces these acquired mental defects is not known. The results presented above, namely the inhibition of I NMDA caused by high concentrations of L-Phe, may provide a cellular mechanism whereby hyperphenylalaninemia contributes to the development of mental retardation during PKU.…”

Section: Implications Of I Nmda Regulation By L-phementioning

confidence: 99%

Specific inhibition of N-methyl-D-aspartate receptor function in rat hippocampal neurons by L-phenylalanine at concentrations observed during phenylketonuria

et al. 2002

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PKU, Learning, and models of mental retardation

Cited by 26 publications

References 43 publications

Cognitive profile of rats exposed to lactational hyperphenylalaninemia: Correspondence with human mental retardation

Cognitive profile of rats exposed to lactational hyperphenylalaninemia: Correspondence with human mental retardation

Biological Contribution to Social Influences on Alcohol Drinking: Evidence from Animal Models

Specific inhibition of N-methyl-D-aspartate receptor function in rat hippocampal neurons by L-phenylalanine at concentrations observed during phenylketonuria

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